自噬
生物
细胞生物学
癌症研究
细胞器
癌细胞
癌症
机制(生物学)
DNA损伤
程序性细胞死亡
细胞
DNA
生物化学
遗传学
细胞凋亡
哲学
认识论
作者
Naiara Santana-Codina,Joseph D. Mancias,Alec C. Kimmelman
标识
DOI:10.1146/annurev-cancerbio-041816-122338
摘要
Autophagy is a highly conserved and regulated process that targets proteins and damaged organelles for lysosomal degradation to maintain cell metabolism, genomic integrity, and cell survival. The role of autophagy in cancer is dynamic and depends, in part, on tumor type and stage. Although autophagy constrains tumor initiation in normal tissue, some tumors rely on autophagy for tumor promotion and maintenance. Studies in genetically engineered mouse models support the idea that autophagy can constrain tumor initiation by regulating DNA damage and oxidative stress. In established tumors, autophagy can also be required for tumor maintenance, allowing tumors to survive environmental stress and providing intermediates for cell metabolism. Autophagy can also be induced in response to chemotherapeutics, acting as a drug-resistance mechanism. Therefore, targeting autophagy is an attractive cancer therapeutic option currently undergoing validation in clinical trials.
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